Mutation is not constant throughout geological history. Natural selection is not constant throughout geological history.
The rates of mutation depend on numerous factors almost none of which are without change. The rate of cell division alone depends on many factors, both external (like temperature or food availability) and species-specific (like the general length of the cell’s life cycle, or the replication error correction mechanisms in place). For multicellular organisms, the rate of reproduction also does. Solar radiation is not constant, neither is the composition of the atmosphere or the oceans.
Natural selection depends on the environment in the broadest sense: physical, chemical, and what other organisms it is shared with. None of those constituents of the environment are constant.
Granted, I am not well-read in biological literature of any variety, so I shan’t presume one way or another as to the general assumptions among people of the field, and instead ask you, as someone who apparently has some grasp of the consensus: What gives you the impression that so obviously false things are yet generally assumed?
That’s just an absurdly circular re-assertion and no explanation, because there’s simply no need for a binary classification. That’s not how real biochemists work.
On top of that, virtually everyone who has done the most basic molecular biology is familiar with phenomena like satellite colonies, in which bacteria are growing without the beta-lactamase because a central colony is excreting it. Is that a function?
Look at Axe’s own barnase paper. Why does it have enzymatic assays?
It’s simply a circular assertion, not an explanation.
There’s no need with enzymatic assays.
Why? Axe’s alleged purpose was to determine whether it evolved, not how researchers exploit it in the lab.
Um, I could do the same thing, and say you are falling back to saying the reviewers really missed many important mistakes in Axe’s paper! Which do you think is more likely? I think the reviewers were more likely competent, and did their job.
So Axe did pick “a low selection threshold”, he said, now do you have evidence that his threshold wasn’t low enough?
Those are almost entirely solicited pieces, so you’re wrong yet again.
For extraordinary cases, this is handled through letters to the editor. The editor is not obligated to publish them. Publishing them is very rare.
So, how has that evidence changed your position?
Fit for what? Have you forgotten that you are claiming that this was about its evolution? How would either of you know if there is any threshhold in the wild?
Hint: your position is absurd because of diffusion.
You are parroting, because you don’t explain why any binary lab classification is evolutionarily relevant, because you can’t. Hint: diffusion of the antibiotic.
He hasn’t followed up this paper in any way.
Not according to them!
You seem to lack even a Wikipedia-level of knowledge regarding these people, yet you reflexively defend them at every turn. Why?
Yes, here is the link I was referring to, Axe responded to four objections there, and I myself responded to Art here on what I gather were his central objections, and he apparently left off responding to me…
This is actually great. It is obvious, of course, that followers of the DI don’t really understand much of what they read from either side. They just notice that one of their heroes has written something, literally anything, in response to an “evolutionist”, and just assume or take on faith that this “something” actually addresses the argument that is being responded to (when, in fact, it almost never does.) But we don’t often get as stark an illustration of this phenomenon as you have just given us right here. Thanks.
You can utter whatever words occur to you. Are they of any probative value? The answer is no.
So that’s it. Into the “he doesn’t know how to respond bin” it goes.
Yes. It’s the fact that his experiment is carried out at the MIC for the temperature sensitive “reference sequence” he constructed. Minimum Inhibitory Concentration.
That’s the lowest concentration of antibiotic that prevents growth of bacteria entirely.
Enzymes need a certain level of activity to counteract that level of antibiotic. If the enzymes aren’t fast enough at degrading the antibiotic, the bacteria are killed before the enzyme has removed enough of it for the bacteria to survive and start growing and dividing.
At lower concentrations of antibiotic (below the MIC) their growth rates are merely reduced (they grow slowly, instead of not growing at all), and hence even lower levels of enzymatic activity still produces fitness advantages at concentrations below the MIC. So enzymes even more weakly active, but still functional, would be scored nonfunctional in his experiment. His experiment therefore fails to capture the full breadth of functional enzymes, which inflates his calculated fraction of sequence space that corresponds to functional enzymes.
They very clearly did, and I have more than enough expertise to be a reviewer myself!
It would seem that if you were interested in a discussion instead of debate, you would have at a minimum questioned me about my expertise about it instead of engaging in circular assertions.
So are you here for discussion, or just debate from aggressive ignorance?
That the review process failed completely in this case. It happens.
Reviewers can assign students and postdocs to do reviews on the down-low. It happens.
Editors can approve publication with a single review.
You have no evidentiary basis for that thought. Nor does Axe. Even if you’re right and I’m wrong, there’s no explanation for the absence of any followup.
Well, why did you omit the rest of what I wrote? “Axe responded to four objections there, and I myself responded to Art here on what I gather were his central objections, and he apparently left off responding to me…”
Axe did respond to Art, I responded to Art, I should mention I posted some excerpts from Axe’s response, that was to motivate discussion, actually, and this is your reply? Art punted, you punt, this does not do your cause any credit. Please respond to Axe’s points, and respond where Art left off to me if you like…
I read enough to find a clear counterexample to your claim. You did not show me how my claim is false, and I don’t think reading further is going to refute the counterexample. And is your claim that the researcher had a way to detect any new function? How could you possibly test for all possible functions?
Um, why don’t you quote the paper under discussion, and show what new functions arrived there? But the question at issue is how often do new functions arise from gene fusion, let’s focus on the rate here.
So how is the proportion of 1 in ~300 000 any sort of solid result? Mutations such as Axe investigated give rise to “molecular clocks”, so we can get a reasonable idea of what evolution can do, with such mutations.
What evidence can you present for this claim, though? From ScienceDirect: “The normal mutation rate is often stated as 10−7 to 10−8 per nucleotide per cell division. This estimate applies, of course, only to small-scale mutations, which produce mis-sense, nonsense or frameshift changes.” This indicates that what is generally thought of as a mutation refers to small-scale mutations, not gene insertions/deletions.
Again I ask, what process other than mutation/selection do you suggest for this? Or if you are suggesting that mutation rates changed dramatically, what evidence do we have for this? And we need to inform the people who investigate molecular clocks.
Certainly! Doug Axe explains: “The remedy is to use a different starting sequence. Specifically, we need the starting sequence to be of the same quality that we intend to require of mutant sequences in order for them to be accepted. Otherwise the mismatch in quality will skew our results.”
“The first problem with Objection 3, then, is that it fails to recognize the importance of applying the same quality standard to the starting sequence that will be applied to the mutants derived from it. Objection 3 focuses on the fact that I used a weakly functional starting sequence without recognizing that this was called for by the fact that weakly functional variants of that sequence were accepted as ‘functional’.”
Yes, but it doesn’t seem to be addressing Axe’s reply.
You’re not making any sense at all. Seriously, are you, like Axe, trying to just obfuscate here because you dislike where this is going? Please be honest.
The experimental method is explained perfectly well in the article. Sorry, this response of yours is completely ineffective. You don’t have “a counterexample”(to what?), I already discounted the self-rescue in the number in the pandasthumb article I wrote. There were six functional proteins found, of which one was the self-rescue you described in your quote. The other five new proteins are not self-rescue clones, and therefore count.
So the number is 5 / 1.65 million = 1 in 330 000 gene fusions result in a new functional protein. A number fantastically more frequent than Axe’s very poorly estimated number of 10-77. Since gene fusions are an observed fact, evolution doesn’t need to search 1077 random sequences to find a new functional protein.
No that isn’t my claim at all, why would it be? Please try to make sense.
If you read the article I wrote, again, for comprehension—you should be able to understand how Rawcliffe detected new functional proteins in his experiments. He uses knock-out strains, that is strains with genes with known and essential (necessary for growth and division) functions that have been deleted (“auxotrophic” strains of E coli).
The cells therefore can’t grow unless they are provided a new gene that can compensate for the one that was knocked out. Rawcliffe then screens the library of random fusion proteins to see whether any of these can compensate for the knocked out gene by giving these fusion genes to the bacteria and looks for whether colonies form on agar plates. If they do, it means a knock-out strain has somehow gained the ability to grow and divide because the novel fusion gene could compensate for the one that was knocked out.
I take it you don’t need help to click on a link and read for yourself? If you can’t be bothered doing that, I can’t be bothered doing it for you.
Regardless, the take-home message from those papers is really simple. The evolutionary gains of novel functional genes through mutations causing gene-fusion were directly observed, and therefore whatever the sort of “average” probability of those events are across all living organisms on Earth, it’s demonstrably frequent enough for new genes to evolve even within human lifetimes. In fact some times in a few weeks or months of a laboratory experiments.
Axe tries to argue that novel functional gene gains should be considered so fantastically rare as to be expected never to occur in the history of life. And yet that is demonstrably not the case.
By it being empirically derived in a clear and relatively simple set of experiments. Transformation of one hundred and seven different auxotrophic strains of bacteria with a large library of random fusion proteins.
Non-synonymous mutation rates vary across all phyla, rather enormously, too. What are you even trying to say? Please elaborate. Think more deeply of what specifically you want to say, then write it, let it sit, then try to determine whether it makes sense, edit it if not, then post. Try harder to make sense.
Yes he says those words, and those words were refuted by my explanation. Quoting his explanation back to me does not refute my explanation for why he is wrong to say those words. There is no such thing as truth-through-repetition.
Read for comprehension.
Actually you know what? I am now satisifed with our exchange. This discussion is over and I have conclusively refuted Axe’s pathetic excuses in a way where I have become utterly convinced that a normally intelligent person with genuine curiosty and a willingness to consider what each side says will come to my side on this. I don’t even care what you believe.
What would “it” be? Bechly assumes that the probability of a new body plan emerging, in an evolutionary model, is constant over time, and so the non-constancy observed falsifies evolution. If you just substitute divine saltation for evolution, with the same assumption about rate, the observed non-constancy falsifies that too. But Bechly assumes that evolution must be constant but divine saltation stopped recently, so everything is fine. But does that in fact make sense?
In order for that absence to be surprising, we have to assume that new body plan events would be expected in the last 5 million years. This requires that they are common enough that some are expected in any 5-million-year period and that those events are distributed fairly evenly through earth history.
Yes, probabilities change over time. The period immediately following a mass extinction, for example, is much more likely to feature such new body plans than a time of low environmental disturbance. Do you know the term “adaptive radiation”? Nothing other than mutation and selection is necessary, but you have to realize that selection is a response to environment, and environment changes. Sometimes quickly, sometimes slowly.
You’re talking about rarefaction curves. They generally are applied to single horizons, not the entire history of life. Not really relevant here.
We could argue about what the Cambrian explosion actually is, but you aren’t equipped. I recommend a fine book, The Cambrian Explosion, by Doug Erwin and Jim Valentine. Still the best single work on the subject. Anyway, the argument in science isn’t about whether the explosion is real but about just what it is and how much time it took. It’s clear that it took lots more than 5 million years, though. More like 30 or 40.
New samples of what, exactly? New Cambrian organisms? Sure. New fossils of other ages? Also sure. One of my favorite factoids: 50% of all dinosaur genera are known from only a single specimen. What does that tell you about the completeness of the known fossil record?
Have you noticed that this definition, which is indeed the most commonly used one, is entirely different from the one Bechly used? Under that definition, all vertebrates have the same Bauplan, so the evolution of whales isn’t an example of a new body plan at all. Baupläne differ among phyla.
I swear you don’t read anything you cite and you don’t read anything anyone says to you.
I notice here there is also an “Amendments and Corrections” section in Nature, which is just that. There is actually one retraction! And the Commentary section of Science has a “Letter”, presumably somebody wrote to them. In all the journals I used to read, there was a “Letters to the editor” section of some sort, and discussions would ensue. I begin to think you all are blowing smoke in my face.
Fit for survival! That’s certainly part of evolution. I mean, seriously? So researchers try and pick a level of antibiotics, for instance, that they think would distinguish between fit and unfit bacteria. I don’t think that’s absurd.
Axe writes: “In the work described in the 2004 JMB paper, I chose to apply the lowest reasonable standard of function knowing this would produce the highest reasonable value for P, which in turn provides the most optimistic assessment of the feasibility of evolving new protein folds. … the method I used was deliberately generous toward Darwinism.”
So a function is there, or it is not, this is binary, and evolutionarily applicable. That is not to say that his detection method was perfect! But it does seem a reasonable approach. Axe is also setting out to be generous here, picking the lowest reasonable standard for a threshold.
From the abstract of the PLOS paper:
: “The study of protein evolution is complicated by the vast size of protein sequence space, the huge number of possible protein folds, and the extraordinary complexity of the causal relationships between protein sequence, structure, and function. Much simpler model constructs may therefore provide an attractive complement to experimental studies in this area.”
This would be a follow-up to his 2004 paper.
Well, the Wikipedia article notes that the article’s neutrality is disputed, and that its “tone or style may not reflect the encyclopedic tone used on Wikipedia”. I would therefore not be inclined to trust it so much. Biologic still lists its address as being in Redmond, that indicates they do have an office there, and they make no claim that I can find, to having lab facilities, nor can I find a lab picture on their website.
Because I find ID arguments compelling, and even defensible, even here! I am enjoying this discussion, it’s helping me to confirm that there is good reason for my views.
I appreciate the clarification, and I can’t seem to find the link to that article, if someone could post that, it would be helpful.
I still need a rate of gene-fusion events, and the evidence for a rate. Saying, as you did, that “There is no such thing as THE rate of insertion/deletions mutations. They can vary massively depending on species and environmental context” is not an answer.
People investigate molecular clocks, and various ways to calibrate them. So we can get an idea of how frequently mutations such as Axe investigated may occur. I’m unsure why this is unclear.
I did not repost his explanation, though. I didn’t do that. I posted more detail from his reply, that you somehow think is a copy of what I posted earlier. Points you have not addressed.
And you were the one scolding me about reading comprehension…
I somehow missed how you replied to my latest quote from Axe. Saying it was a repost, and stuff.
So again, how many other papers in this field did you read before trying to defend Axe with meaningless, circular assertions and cut/pasting?
I’m pretty sure that the thing that you are claiming to be “actually rare” is not the mutation rate.
Let’s see if your faith is strong enough to make a concrete prediction instead of retrospective handwaving: if one screens a library of immunoglobulin sequences from an unimmunized mouse, what fraction do you predict will have a particular enzymatic activity?
